Angiotensin-converting Enzyme Inhibitors

Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find the ACE Inhibitors article more useful, or one of our other health articles.

This family of drugs inhibits the conversion of angiotensin I to angiotensin II by inhibiting angiotensin-converting enzyme (ACE). Angiotensin II has various functions including:

Promoting vasoconstriction - through stimulation of the sympathetic nervous system, and the release of aldosterone and vasopressin.

Renal changes - some of which are through the actions of aldosterone (with salt and water retention) and others which may be caused directly - eg, renal vasoconstriction.

Cardiac and vascular remodelling - through the actions of growth factors and increased afterload.

This leads to hypertension and the complications of hypertension, such as left ventricular hypertrophy. ACE inhibitors induce vasodilatation which will improve cardiac output (by reducing afterload) and enhance the renal excretion of salt and water. Most ACE inhibitors are prodrugs which are metabolised in the liver to active metabolites. All are excreted by the kidney, and need careful titration in renal impairment.[1]Under normal circumstances, ACE also inactivates bradykinin; thus, ACE inhibition is associated with increased levels of bradykinin and this is thought to underly the ACE inhibitor-associated cough.

Hypertension: recommended first-line antihypertensive in those with diabetes and in younger (<55 years) patients with hypertension, and second-line for other patients if blood pressure (BP) is not adequately controlled on thiazide or a calcium-channel blocker (or if these drugs are not tolerated or are contra-indicated). See separate article Management of Hypertension.

Heart failure: (particularly in patients with left ventricular dysfunction); reduces both mortality and hospital admissions in these patients. More recently data are emerging that ACE inhibitors are also beneficial in patients with heart failure and normal left ventricular systolic function. See separate article Heart Failure Management.

Post-myocardial infarction (MI): ACE inhibitors reduce ischaemic events, mortality and hospital admissions (heart failure or further MI) in this group of patients. There is good evidence to suggest that they should be started early.

Diabetic nephropathy: as well as lowering BP, ACE inhibitors reduce the rate of albumin excretion in normotensive patients with diabetes (types 1 and 2). There is reduced mortality (all causes).[3]

First-dose hypotension - minimise this by stopping or reducing loop diuretics for 24 hours before starting and give a small trial dose, and/or take tablet immediately at bedtime. Consider initiation under specialised supervision.[9]

Initiation

Always check U&E and creatinine before starting.

Assess the patient for likely problems - consider whether ACE inhibitors may be better started in hospital - eg, in patients with high risk of first-dose hypotension, hyperkalaemia or renal failure:[9]

If on high-dose diuretics (>80 mg furosemide/day) - reduce or stop diuretics, if possible a day or two before starting an ACE inhibitor, to reduce the risk of first-dose hypotension. If this is not possible - monitor BP for two hours post-dose.

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